Movement disorders are neurologic syndromes characterized by either an excess or a paucity of movement. These disorders affect approximately two million Americans, including over one million suffering from benign essential tremor, and half a million suffering from Parkinson's Disease. A substantial percentage of those afflicted with movement disorders experience a significant decrease in quality of life, suffering such problems as incapacitating tremor, limited mobility, bradykinesia (difficulty consciously initiating movement), dysarthria (difficulty with speech), and consequent social isolation. The etiology of many movement disorders, e.g., benign essential tremor, is poorly understood. For other movement disorders, e.g., Parkinson's disease, the mechanism of the disorder and brain cells affected have been identified, but even with optimal care the disease may not be reversed and may even continue to progress.
Parkinson's Disease is caused by a gradual loss of dopaminergic (i.e., dopamine-secreting) neurons in the substantia nigra. Consequently, levels of dopamine decrease in the striatum (i.e., the putamen and the caudate nucleus). Although dopamine has both excitatory and inhibitory effects on the striatum, the predominant effect of the loss of dopamine is decreased inhibition (by GABA) of the internal segment of the globus pallidus. This leads to increased GABA output from the internal segment of the globus pallidus, which inhibits the ventrolateral thalamus. This leads in turn to decreased inhibition of (and ultimately decreased control over) the motor cortex. The subthalamic nucleus appears to increase its activity in Parkinson's Disease as well, and this is believed to contribute to the symptoms of the disease.
Essential Tremor (ET), a.k.a., Benign Essential Tremor, is the most common movement disorder. It is a syndrome characterized by a slowly progressive postural and/or kinetic tremor, usually affecting both upper extremities. The prevalence of ET in the US is estimated at 0.3–5.6% of the general population. A 45-year study of ET in Rochester, Minn. reported an age- and gender-adjusted prevalence of 305.6 per 100,000 and an incidence of incidence of 23.7 per 100,000.
ET affects both sexes equally. The prevalence of ET increases with age. There are bimodal peaks of onset—one in late adolescence to early adulthood and a second peak in older adulthood. The mean age at presentation is 35–45 years. ET usually presents by 65 years of age and virtually always by 70 years. Tremor amplitude slowly increases over time. Tremor frequency decreases with increasing age. An 8–12 Hz tremor is seen in young adults and a 6–8 Hz tremor is seen in the elderly. Although ET is progressive, no association has been found between age of onset and severity of disability.
Mortality rates are not increased in ET. However, disability from ET is common. Significant changes in livelihood and socializing are reported by 85% of individuals with ET, and 15% report being seriously disabled due to ET. Decreased quality of life results from both loss of function and embarrassment. In a study of hereditary ET, 60% did not seek employment; 25% changed jobs or took early retirement; 65% did not dine out; 30% did not attend parties, shop alone, partake of a favorite hobby or sport, or use public transportation; and 20% stopped driving.
A number of US patents have addressed using electrical and/or drug stimulation to increase and/or decrease excitement of various brain structures to treat movement disorders. See, for instance, U.S. Pat. Nos. 6,094,598; 5,833,709; 5,716,377; 5,832,932; 5,711,316; 5,792,186; and 6,227,203. Portions of these seven patents are identical, and they teach both increasing excitement/activity (or decreasing inhibition) and decreasing excitement/activity (or increasing inhibition) of the ventrolateral (VL) thalamus, the globus pallidus interna (GPi), the substantia nigra reticulata (SNr), the subthalamic nucleus (STN), the globus pallidus externa (GPe), the neostriatum, and the striatum. Also taught is increasing excitement of the motor cortex, stiatopallidal fiber pathway, GPe to STN fiber pathway, pallido-thalamic axons, putamen to GPe fibers, and subthalamo-pallidal tracts. U.S. Pat. No. 6,356,784 teaches increasing the activity of the pendunolopontine nucleus (PPN) to treat movement disorders such as Parkinson's Disease, while decreasing PPN activity is used for treating other conditions such as schizophrenia.
While these various treatment locations, methods, and systems exist, the inventors believe that enhanced systems, alternative locations, and modified methods will lead to improved treatment of movement disorders.